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Estradiol treatment attenuates high fat diet-induced microgliosis in ovariectomized rats.
Hormones and Behavior ( IF 3.5 ) Pub Date : 2020-01-13 , DOI: 10.1016/j.yhbeh.2020.104675
Michael J Butler 1 , Alexis A Perrini 2 , Lisa A Eckel 2
Affiliation  

Consumption of a high fat diet (HFD) increases circulating free fatty acids, which can enter the brain and promote a state of microgliosis, as defined by a change in microglia number and/or morphology. Most studies investigating diet-induced microgliosis have been conducted in male rodents despite well-documented sex differences in the neural control of food intake and neuroimmune signaling. This highlights the need to investigate how sex hormones may modulate the behavioral and cellular response to HFD consumption. Estradiol is of particular interest since it exerts a potent anorexigenic effect and has both anti-inflammatory and neuroprotective effects in the brain. As such, the aim of the current study was to investigate whether estradiol attenuates the development of HFD-induced microgliosis in female rats. Estradiol- and vehicle-treated ovariectomized rats were fed either a low-fat chow diet or a 60% HFD for 4 days, after which they were perfused and brain sections were processed via immunohistochemistry for microglia-specific Iba1 protein. Four days of HFD consumption promoted microgliosis, as measured via an increase in the number of microglia in the arcuate nucleus (ARC) of the hypothalamus and nucleus of the solitary tract (NTS), and a decrease in microglial branching in the ARC, NTS, lateral hypothalamus (LH), and ventromedial hypothalamus. Estradiol replacement attenuated the HFD-induced changes in microglia accumulation and morphology in the ARC, LH, and NTS. We conclude that estradiol has protective effects against HFD-induced microgliosis in a region-specific manner in hypothalamic and hindbrain areas implicated in the neural control of food intake.

中文翻译:

雌二醇治疗可减轻卵巢切除大鼠的高脂饮食诱导的小胶质细胞增生。

食用高脂肪饮食(HFD)会增加循环中的游离脂肪酸,脂肪酸可进入大脑并促进小胶质细胞增生,这是由小胶质细胞数量和/或形态的改变所定义的。尽管在饮食控制和神经免疫信号传导的神经控制方面有充分的性别差异,但大多数调查饮食引起的小胶质细胞增生的研究都是在雄性啮齿动物上进行的。这突出了需要研究性激素如何调节对HFD摄入的行为和细胞反应。雌二醇特别令人感兴趣,因为它在脑中发挥了强效的厌食作用,并具有抗炎和神经保护作用。因此,本研究的目的是研究雌二醇是否能减轻雌性大鼠HFD诱导的小胶质细胞增生的发展。雌二醇和媒介物处理的去卵巢大鼠被喂以低脂食物或60%HFD饮食4天,然后进行灌流,并通过免疫组织化学处理脑切片以检测小胶质细胞特异性Iba1蛋白。通过测量下丘脑弓状核(ARC)和孤立道(NTS)核的小胶质细胞数量增加,以及ARC,NTS,下丘脑外侧(LH)和腹膜下丘脑。雌二醇替代减弱了HFD诱导的ARC,LH和NTS中小胶质细胞积累和形态的变化。
更新日期:2020-01-13
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